Steroid binding proteins

Because non-genomic pathways include any mechanism that is not a genomic effect, there are various non-genomic pathways. However, all of these pathways are mediated by some type of steroid hormone receptor found at the plasma membrane. [13] Ion channels, transporters, G-protein coupled receptors (GPCR), and membrane fluidity have all been shown to be affected by steroid hormones. [9] Of these, GPCR linked proteins are the most more information on these proteins and pathways, visit the steroid hormone receptor page.

C/EBPβ and δ are transiently induced during the early stages of adipocyte differentiation ( adipogenesis ), while C/EBPα is upregulated during the terminal stages of adipogenesis. In vitro and in vivo studies have demonstrated that each plays an important role in this process. For example, Murine Embryonic Fibroblasts (MEFs) from mice lacking both C/EBPβ and C/EBPδ show impaired adipocyte differentiation in response to adipogenic stimuli. [4] In contrast, ectopic expression of C/EBPβ and δ in 3T3-L1 preadipocytes promotes adipogenesis, even in the absence of adipogenic stimuli. [5] [6] C/EBPβ and δ promote adipogenesis, at least in part by inducing the expression of the "master" adipogenic transcription factors C/EBPα and PPARγ .

Anabolic
steroids are synthetic substances related to male sex hormones
(androgens). Although it is illegal in the United States to possess or
distribute anabolic steroids for nonmedical use, a "black
market" for them exists, and many amateur and professional athletes
take them to enhance performance. In many cases, the athletes take doses
that are extremely high—perhaps 100 times the doses that might be
prescribed for medical use. As a result, they put themselves in real
danger of short-term and long-term health problems. Blood testing, as has
been used in the Olympic Games, can detect, identify, and quantify the
presence of anabolic steroids in the blood of athletes, which can lead to
the disqualification of an athlete.

Cells of the zona fasciculata and zona reticularis lack aldosterone synthase (CYP11B2) that converts
corticosterone to aldosterone, and thus these tissues produce only the weak mineralocorticoid corticosterone.
However, both these zones do contain the CYP17A1 missing in zona glomerulosa and thus produce the major
glucocorticoid, cortisol. Zona fasciculata and zona reticularis
cells also contain CYP17A1, whose 17,20-lyase activity is responsible for producing the androgens,
dehydroepiandosterone (DHEA) and androstenedione. Thus, fasciculata and reticularis cells can make
corticosteroids and the adrenal androgens, but not aldosterone.

Steroid binding proteins

Cells of the zona fasciculata and zona reticularis lack aldosterone synthase (CYP11B2) that converts
corticosterone to aldosterone, and thus these tissues produce only the weak mineralocorticoid corticosterone.
However, both these zones do contain the CYP17A1 missing in zona glomerulosa and thus produce the major
glucocorticoid, cortisol. Zona fasciculata and zona reticularis
cells also contain CYP17A1, whose 17,20-lyase activity is responsible for producing the androgens,
dehydroepiandosterone (DHEA) and androstenedione. Thus, fasciculata and reticularis cells can make
corticosteroids and the adrenal androgens, but not aldosterone.